ArticleBlood2010
Identification of early growth response protein 1 (EGR-1) as a novel target for JUN-induced apoptosis in multiple myeloma.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 86 citations in OpenAlex.
- Mutational Spectrum, Copy Number Changes, and Outcome: Results of a Sequencing Study of Patients With Newly Diagnosed Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Trial
- The JNK2-microbiome axis modulates gut barrier integrity through microbial acetate.Gut microbes · 2026Article
- Multiple myeloma: A tale of deregulated transcription factors.HemaSphere · 2026Review
- Stromal and endothelial transcriptional changes during progression from MGUS to myeloma and after treatment response.Nature communications · 2026Article
- Identification of BRCA1-Associated RING Domain 1 Mutation as a Novel Indicator for Constructing a Prognostic Nomogram in Multiple Myeloma: A Retrospective Single-Center Study.Cancer management and research · 2026Article
- The de novo DNA methyltransferase 3B is a novel epigenetic regulator of MYC in multiple myeloma, representing a promising therapeutic target to counter relapse.Journal of experimental & clinical cancer research : CR · 2025Article
- PMF-GRN: a variational inference approach to single-cell gene regulatory network inference using probabilistic matrix factorization.Genome biology · 2024Article
- Distinct transcriptomes and autocrine cytokines underpin maturation and survival of antibody-secreting cells in systemic lupus erythematosus.Nature communications · 2024Article
- Network pharmacology study to explore the multiple molecular mechanism of SH003 in the treatment of non-small cell lung cancer.BMC complementary medicine and therapies · 2024Article
- Evaluation of Genes and Molecular Pathways Involved in the Progression of Monoclonal Gammopathy of Undetermined Significance (MGUS) to Multiple Myeloma: A Systems Biology Approach.Molecular biotechnology · 2023Article
- N6-methyladenosine reader YTHDF2 promotes multiple myeloma cell proliferation through EGR1/p21Oncogene · 2023Article
- Article
- Comprehensive analysis of prognosis of cuproptosis-related oxidative stress genes in multiple myeloma.Frontiers in genetics · 2023Article
- Modulation of viral replication, apoptosis and antiviral response by induction and mutual regulation of EGR and AP-1 family genes during coronavirus infection.Emerging microbes & infections · 2022Article
- Article
- Early Growth Response Factor 1 in Aging Hematopoietic Stem Cells and Leukemia.Frontiers in cell and developmental biology · 2022Review
- Prognostic and predictive biomarker developments in multiple myeloma.Journal of hematology & oncology · 2021Review
- EGR1 Addiction in Diffuse Large B-cell Lymphoma.Molecular cancer research : MCR · 2021Article
- PHF19 inhibition as a therapeutic target in multiple myeloma.Current research in translational medicine · 2021Article
- CHEK1 and circCHEK1_246aa evoke chromosomal instability and induce bone lesion formation in multiple myeloma.Molecular cancer · 2021Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Tumor-bone marrow microenvironment interactions in multiple myeloma (MM) are documented to play crucial roles in plasma-cell growth/survival. In vitro coculture of MM cells with osteoclasts supported cell survival and significantly down-regulated JUN expression. JUN expression in myeloma cells from late-stage and high-risk MM was significantly lower than in plasma cells from healthy donors, monoclonal gammopathy of undetermined significance, smoldering MM, and low-risk MM; patients with low-JUN-expressing MM cells had earlier disease-related deaths. JUN overexpression in MM cells induced cell death and growth inhibition and up-regulated expression of early growth response protein 1 (EGR-1), whose low expression also carried unfavorable clinical implications. EGR-1 knockdown in MM cells abrogated JUN overexpression-induced MM cell death and growth inhibition, indicating that EGR-1 acts directly downstream of JUN. JUN modulates myeloma cell apoptosis through interacting with EGR-1, which down-regulates Survivin and triggers caspase signaling. Importantly, high JUN or EGR-1 expression was associated with improved outcome in Total Therapy 3, in which bortezomib is given throughout therapy, versus Total Therapy 2, in which bortezomib is given only at relapse. Consistently, JUN or EGR-1 knockdown in cultured MM cells enhanced their resistance to bortezomib, demonstrating the crucial role of low JUN/EGR-1 expression in MM resistance to bortezomib.
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